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@ARTICLE{Wang:296086,
      author       = {J. Wang and L. Liao and B. Miao$^*$ and B. Yang and B. Li
                      and X. Ma and A. Fitz$^*$ and S. Wu and J. He and Q. Zhang
                      and S. Ji and G. Jin and J. Zhang and Y. Cao and H. Wang and
                      W. Qin and C. Sun$^*$ and R. Bernards and C. Wang},
      title        = {{D}eciphering the role of the {MALT}1-{RC}3{H}1 axis in
                      regulating {GPX}4 protein stability.},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {122},
      number       = {1},
      issn         = {0027-8424},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {DKFZ-2025-00034},
      pages        = {e2419625121},
      year         = {2025},
      note         = {#EA:D250#},
      abstract     = {Ferroptosis, a unique form of iron-dependent cell death
                      triggered by lipid peroxidation accumulation, holds great
                      promise for cancer therapy. Despite the crucial role of GPX4
                      in regulating ferroptosis, our understanding of GPX4 protein
                      regulation remains limited. Through FACS-based genome-wide
                      CRISPR screening, we identified MALT1 as a regulator of GPX4
                      protein. Inhibition of MALT1 expression enhances GPX4
                      ubiquitination-mediated degradation by up-regulating the E3
                      ubiquitin ligase RC3H1. Using both rescue assays and
                      functional genetic screening, we demonstrate that
                      pharmacologically targeting MALT1 triggers ferroptosis in
                      liver cancer cells. Moreover, we show that targeting MALT1
                      synergizes with sorafenib or regorafenib to induce
                      ferroptosis across multiple cancer types. These findings
                      elucidate the modulatory effects of the MALT1-RC3H1 axis on
                      GPX4 stability, revealing a molecular mechanism that could
                      be exploited to induce ferroptosis for cancer therapy.},
      keywords     = {Humans / Phospholipid Hydroperoxide Glutathione Peroxidase:
                      metabolism / Phospholipid Hydroperoxide Glutathione
                      Peroxidase: genetics / Ferroptosis: genetics /
                      Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1
                      Protein: metabolism / Mucosa-Associated Lymphoid Tissue
                      Lymphoma Translocation 1 Protein: genetics / Protein
                      Stability / Ubiquitin-Protein Ligases: metabolism /
                      Ubiquitin-Protein Ligases: genetics / Sorafenib:
                      pharmacology / Cell Line, Tumor / Ubiquitination / Liver
                      Neoplasms: metabolism / Liver Neoplasms: genetics / Liver
                      Neoplasms: drug therapy / Liver Neoplasms: pathology /
                      Phenylurea Compounds: pharmacology / Gene Expression
                      Regulation, Neoplastic / Pyridines / GPX4 (Other) / MALT1
                      (Other) / ferroptosis (Other) / liver cancer (Other) /
                      Phospholipid Hydroperoxide Glutathione Peroxidase (NLM
                      Chemicals) / Mucosa-Associated Lymphoid Tissue Lymphoma
                      Translocation 1 Protein (NLM Chemicals) / Ubiquitin-Protein
                      Ligases (NLM Chemicals) / MALT1 protein, human (NLM
                      Chemicals) / Sorafenib (NLM Chemicals) / regorafenib (NLM
                      Chemicals) / Phenylurea Compounds (NLM Chemicals) /
                      Pyridines (NLM Chemicals)},
      cin          = {D250},
      ddc          = {500},
      cid          = {I:(DE-He78)D250-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39739814},
      doi          = {10.1073/pnas.2419625121},
      url          = {https://inrepo02.dkfz.de/record/296086},
}